Journal articles: 'Circulation channels'

1

Земцовский, Aleksey Zemtsovskiy, Мануковский, and Andrey Manukovskiy. "A mathematical model of the aerodynamics of drying chambers with vertical transverse circulation." Forestry Engineering Journal 5, no. 2 (September 24, 2015): 131–37. http://dx.doi.org/10.12737/11987.

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In the article, from the standpoint of aerodynamics considered the concept of a mathematical model of the circulation channels marketing chambers of variable cross section with a vertically transverse circulation. Factors affecting the uniformity of the air flow in the pile of lumber. Developed analytical mathematical model of the motion of drying agent on the side channel of variable cross section. Revealed that the parameters of the lateral channel of the drying chamber of variable cross section does not depend on the temperature and humidity of the circulating air, and hence from the "rigidity" of the drying mode.

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Guntur, Divya, Horst Olschewski, Péter Enyedi, Réka Csáki, Andrea Olschewski, and Chandran Nagaraj. "Revisiting the Large-Conductance Calcium-Activated Potassium (BKCa) Channels in the Pulmonary Circulation." Biomolecules 11, no. 11 (November 3, 2021): 1629. http://dx.doi.org/10.3390/biom11111629.

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Potassium ion concentrations, controlled by ion pumps and potassium channels, predominantly govern a cell′s membrane potential and the tone in the vessels. Calcium-activated potassium channels respond to two different stimuli-changes in voltage and/or changes in intracellular free calcium. Large conductance calcium-activated potassium (BKCa) channels assemble from pore forming and various modulatory and auxiliary subunits. They are of vital significance due to their very high unitary conductance and hence their ability to rapidly cause extreme changes in the membrane potential. The pathophysiology of lung diseases in general and pulmonary hypertension, in particular, show the implication of either decreased expression and partial inactivation of BKCa channel and its subunits or mutations in the genes encoding different subunits of the channel. Signaling molecules, circulating humoral molecules, vasorelaxant agents, etc., have an influence on the open probability of the channel in pulmonary arterial vascular cells. BKCa channel is a possible therapeutic target, aimed to cause vasodilation in constricted or chronically stiffened vessels, as shown in various animal models. This review is a comprehensive collation of studies on BKCa channels in the pulmonary circulation under hypoxia (hypoxic pulmonary vasoconstriction; HPV), lung pathology, and fetal to neonatal transition, emphasising pharmacological interventions as viable therapeutic options.

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Lakshmanan, S. P., and Manmohan Pandey. "Numerical Investigation of Startup Instabilities in Parallel-Channel Natural Circulation Boiling Systems." Science and Technology of Nuclear Installations 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/574195.

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The behaviour of a parallel-channel natural circulation boiling water reactor under a low-pressure low-power startup condition has been studied numerically (using RELAP5) and compared with its scaled model. The parallel-channel RELAP5 model is an extension of a single-channel model developed and validated with experimental results. Existence of in-phase and out-of-phase flashing instabilities in the parallel-channel systems is investigated through simulations under equal and unequal power boundary conditions in the channels. The effect of flow resistance on Type-I oscillations is explored. For nonidentical condition in the channels, the flow fluctuations in the parallel-channel systems are found to be out-of-phase.

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4

Li, Chunyan, and James O’Donnell. "The Effect of Channel Length on the Residual Circulation in Tidally Dominated Channels." Journal of Physical Oceanography 35, no. 10 (October 1, 2005): 1826–40. http://dx.doi.org/10.1175/jpo2804.1.

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Abstract With an analytic model, this paper describes the subtidal circulation in tidally dominated channels of different lengths, with arbitrary lateral depth variations. The focus is on an important parameter associated with the reversal of the exchange flows. This parameter (δ) is defined as the ratio between the channel length and one-quarter of the tidal wavelength, which is determined by water depth and tidal frequency. In this study, a standard bottom drag coefficient, CD = 0.0025, is used. For a channel with δ smaller than 0.6–0.7 (short channels), the exchange flow at the open end has an inward transport in deep water and an outward transport in shallow water. This situation is just the opposite of channels with a δ value larger than 0.6–0.7 (long channels). For a channel with a δ value of about 0.35–0.5, the exchange flow at the open end reaches the maximum of a short channel. For a channel with a δ value of about 0.85–1.0, the exchange flow at the open end reaches the maximum of a long channel, with the inward flux of water occurring over the shoal area and the outward flow in the deep-water area. However, near the closed end of a long channel, the exchange flow appears as that in a short channel—that is, the exchange flow changes direction along the channel from the head to the open end of the channel. For a channel with a δ value of about 0.6–0.7, the tidally induced subtidal exchange flow at the open end reaches its minimum when there is little flow across the open end and the water residence time reaches its maximum. The mean sea level increases toward the closed end for all δ values. However, the spatial gradient of the mean sea level in a short channel is much smaller than that of a long channel. The differences between short and long channels are caused by a shift in dynamical balance of momentum or, equivalently, a change in tidal wave characteristics from a progressive wave to a standing wave.

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Faraci, Frank M., and Christopher G. Sobey. "POTASSIUM CHANNELS AND THE CEREBRAL CIRCULATION." Clinical and Experimental Pharmacology and Physiology 23, no. 12 (December 1996): 1091–95. http://dx.doi.org/10.1111/j.1440-1681.1996.tb01175.x.

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Dellsperger, Kevin C. "POTASSIUM CHANNELS AND THE CORONARY CIRCULATION." Clinical and Experimental Pharmacology and Physiology 23, no. 12 (December 1996): 1096–101. http://dx.doi.org/10.1111/j.1440-1681.1996.tb01176.x.

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7

Kitazano, Takanari, Setsuro Ibayashi, Tetsuhiko Nagao, Hitonori Takaba, and Masatoshi Fujishima. "Potassium channels and the cerebral circulation." Nosotchu 20, no. 2 (1998): 225–38. http://dx.doi.org/10.3995/jstroke.20.225.

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8

Popa, Ioana. "Translation channels." Target. International Journal of Translation Studies 18, no. 2 (December 31, 2006): 205–28. http://dx.doi.org/10.1075/target.18.2.02pop.

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Focusing on a comparative analysis of the translations in French of literary works from four Eastern European countries (Poland, Czechoslovakia, Hungary and Romania) during the communist period, this article examines the political stakes of the international circulation of literary texts. More precisely, it proposes a model for describing the different modalities of international circulation—referred to here as translation channels—based on the statistical analysis of a relevant set of variables. These channels allow us to present a gradation of the degree of politicization and institutionalization of the literary transfer, and to go well beyond an analysis in terms of the undifferentiated flow of imported books or the simple opposition of authorized vs. unauthorized translations or submissive vs. dissenting writers.

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9

FARACI, FRANK M., and DONALD D. HEISTAD. "Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels." Physiological Reviews 78, no. 1 (January 1, 1998): 53–97. http://dx.doi.org/10.1152/physrev.1998.78.1.53.

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Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes.

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10

Schulz, Elisabeth, Henk M. Schuttelaars, Ulf Gräwe, and Hans Burchard. "Impact of the Depth-to-Width Ratio of Periodically Stratified Tidal Channels on the Estuarine Circulation." Journal of Physical Oceanography 45, no. 8 (August 2015): 2048–69. http://dx.doi.org/10.1175/jpo-d-14-0084.1.

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AbstractThe dependency of the estuarine circulation on the depth-to-width ratio of a periodically, weakly stratified tidal estuary is systematically investigated here for the first time. Currents, salinity, and other properties are simulated by means of the General Estuarine Transport Model (GETM) in cross-sectional slice mode, applying a symmetric Gaussian-shaped depth profile. The width is varied over four orders of magnitude. The individual along-channel circulation contributions from tidal straining, gravitation, advection, etc., are calculated and the impact of the depth-to-width ratio on their intensity is presented and elucidated. It is found that the estuarine circulation exhibits a distinct maximum in medium-wide channels (intermediate depth-to-width ratio depending on various parameters), which is caused by a maximum of the tidal straining contribution. This maximum is related to a strong tidal asymmetry of eddy viscosity and shear created by secondary strain-induced periodic stratification (2SIPS): in medium channels, transverse circulation generated by lateral density gradients due to laterally differential longitudinal advection induces stable stratification at the end of the flood phase, which is further increased during ebb by longitudinal straining (SIPS). Thus, eddy viscosity is low and shear is strong in the entire ebb phase. During flood, SIPS decreases the stratification so that eddy viscosity is high and shear is weak. The circulation resulting from this viscosity–shear correlation, the tidal straining circulation, is oriented like the classical, gravitational circulation, with riverine outflow at the surface and oceanic inflow close to the bottom. In medium channels, it is about 5 times as strong as in wide (quasi one-dimensional) channels, in which 2SIPS is negligible.

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11

Mauritzen, C., J. Price, T. Sanford, and D. Torres. "Circulation and mixing in the Faroese Channels." Deep Sea Research Part I: Oceanographic Research Papers 52, no. 6 (June 2005): 883–913. http://dx.doi.org/10.1016/j.dsr.2004.11.018.

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12

Nagaraj, Chandran, Yingji Li, Bi Tang, Natalie Bordag, Divya Guntur, Péter Enyedi, Horst Olschewski, and Andrea Olschewski. "Potassium Channels in the Transition from Fetal to the Neonatal Pulmonary Circulation." International Journal of Molecular Sciences 23, no. 9 (April 23, 2022): 4681. http://dx.doi.org/10.3390/ijms23094681.

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The transition from the fetal to the neonatal circulation includes dilatation of the pulmonary arteries (PA) and closure of the Ductus Arteriosus Botalli (DAB). The resting membrane potential and various potassium channel activities in smooth muscle cells (SMC) from fetal and neonatal PA and DAB obtained from the same species has not been systematically analyzed. The key issue addressed in this paper is how the resting membrane potential and the whole-cell potassium current (IK) change when PASMC or DABSMC are transitioned from hypoxia, reflecting the fetal state, to normoxia, reflecting the post-partal state. Patch-clamp measurements were employed to characterize whole-cell K+ channel activity in fetal and post-partal (newborn) PASMC and DABSMC. The main finding of this paper is that the SMC from both tissues use a similar set of K+ channels (voltage-dependent (Kv), calcium-sensitive (KCa), TASK-1 and probably also TASK-2 channels); however, their activity level depends on the cell type and the oxygen level. Furthermore, we provide the first evidence for pH-sensitive non-inactivating K+ current in newborn DABSMC and PASMC, suggesting physiologically relevant TASK-1 and TASK-2 channel activity, the latter particularly in the Ductus Arteriosus Botalli.

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13

Olschewski, Andrea, Emma L. Veale, Bence M. Nagy, Chandran Nagaraj, Grazyna Kwapiszewska, Fabrice Antigny, Mélanie Lambert, et al. "TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications." European Respiratory Journal 50, no. 5 (November 2017): 1700754. http://dx.doi.org/10.1183/13993003.00754-2017.

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TWIK-related acid-sensitive potassium channel 1 (TASK-1 encoded by KCNK3) belongs to the family of two-pore domain potassium channels. This gene subfamily is constitutively active at physiological resting membrane potentials in excitable cells, including smooth muscle cells, and has been particularly linked to the human pulmonary circulation. TASK-1 channels are sensitive to a wide array of physiological and pharmacological mediators that affect their activity such as unsaturated fatty acids, extracellular pH, hypoxia, anaesthetics and intracellular signalling pathways. Recent studies show that modulation of TASK-1 channels, either directly or indirectly by targeting their regulatory mechanisms, has the potential to control pulmonary arterial tone in humans. Furthermore, mutations in KCNK3 have been identified as a rare cause of both familial and idiopathic pulmonary arterial hypertension. This review summarises our current state of knowledge of the functional role of TASK-1 channels in the pulmonary circulation in health and disease, with special emphasis on current advancements in the field.

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14

Tristani-Firouzi, M., E. B. Martin, S. Tolarova, E. K. Weir, S. L. Archer, and D. N. Cornfield. "Ventilation-induced pulmonary vasodilation at birth is modulated by potassium channel activity." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 6 (December 1, 1996): H2353—H2359. http://dx.doi.org/10.1152/ajpheart.1996.271.6.h2353.

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At birth, pulmonary blood flow rapidly increases 8- to 10-fold, and pulmonary arterial pressure falls by 50% within 24 h. The postnatal adaptation of the pulmonary circulation is mediated, in part, by endothelium-derived nitric oxide (EDNO). Recent studies suggest that EDNO may reduce vascular resistance, in part, by activating K+ channels. We hypothesized that K+ channels modulate the changes in pulmonary hemodynamics associated with birth. To test this hypothesis, we studied the effect of K+ channel inhibition on two separate, but interdependent stimuli: 1) mechanical ventilation with low inspired O2 concentrations (designed to maintain normal fetal blood gas tensions) and 2) mechanical ventilation with high inspired O2 concentrations. Tetraethyl-ammonium (TEA, 1 mg/min for 100 min; n = 5), a nonspecific K+ channel blocker, glibenclamide (Gli, 1 mg/min for 30 min; n = 6), an ATP-sensitive K+ channel blocker, or saline (n = 7) was infused into the left pulmonary artery (LPA) of acutely instrumented fetal lambs. The umbilical-placental circulation remained intact, and lambs were ventilated with 0.10 inspired O2 concentration (FIO2) for 60 min, followed by 1.0 FIO2 for 20 min. Neither TEA nor Gli had an effect on basal pulmonary tone. TEA attenuated the increase in LPA flow and decrease in pulmonary vascular resistance in response to mechanical ventilation with 0.10 and 1.0 FIO2; Gli had no effect. These results support the hypothesis that non-ATP-sensitive K+ channels modulate the transition from fetal to neonatal pulmonary circulation.

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15

Rosenblum, William I. "ATP-Sensitive Potassium Channels in the Cerebral Circulation." Stroke 34, no. 6 (June 2003): 1547–52. http://dx.doi.org/10.1161/01.str.0000070425.98202.b5.

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Roberts, Christine C., Scott A. Roberts, Martin B. Nemer, and Rekha R. Rao. "Circulation within confined droplets in Hele-Shaw channels." Physics of Fluids 26, no. 3 (March 2014): 032105. http://dx.doi.org/10.1063/1.4867695.

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17

Zvirin, Yoram. "Natural circulation loops with parallel channels - transient behavior." Nuclear Engineering and Design 84, no. 1 (January 1985): 73–81. http://dx.doi.org/10.1016/0029-5493(85)90314-0.

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18

Toyoda, K., K. Fujii, S. Ibayashi, T. Kitazono, T. Nagao, and M. Fujishima. "Role of ATP-sensitive potassium channels in brain stem circulation during hypotension." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 3 (September 1, 1997): H1342—H1346. http://dx.doi.org/10.1152/ajpheart.1997.273.3.h1342.

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The basilar artery and its branch arterioles dilate actively in response to a marked decrease in blood pressure and maintain cerebral blood flow (CBF) to the brain stem. We tested the hypothesis that ATP-sensitive potassium (KATP) channels play a role in the autoregulatory responses of the brain stem circulation in vivo. In anesthetized Sprague-Dawley rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and branch arterioles were measured through a cranial window during stepwise hemorrhagic hypotension. During topical application of 10(-6) and 10(-5) mol/l of glibenclamide, a selective KATP-channel blocker, the lower limit of CBF autoregulation shifted upward to 60-75 from 30-45 mmHg in the vehicle group. Glibenclamide significantly impaired the dilator response of small arterioles (baseline diameter 45 +/- 2 microns) throughout hypotension (P < 0.03) but did not impair the dilatation of the basilar artery (247 +/- 3 microns) or large arterioles (99 +/- 4 microns). Thus KATP channels appear to play an important role in the regulation of CBF to the the brain stem during hypotension by mediating the compensatory dilatation of small arterioles. In contrast, these channels may not be a major regulator of the vascular tone of larger arteries during hypotension.

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Reeve, Helen L., E. Kenneth Weir, Stephen L. Archer, and David N. Cornfield. "A maturational shift in pulmonary K+ channels, from Ca2+ sensitive to voltage dependent." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 6 (December 1, 1998): L1019—L1025. http://dx.doi.org/10.1152/ajplung.1998.275.6.l1019.

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The mechanism responsible for the abrupt decrease in resistance of the pulmonary circulation at birth may include changes in the activity of O2-sensitive K+ channels. We characterized the electrophysiological properties of fetal and adult ovine pulmonary arterial (PA) smooth muscle cells (SMCs) using conventional and amphotericin B-perforated patch-clamp techniques. Whole cell K+ currents of fetal PASMCs in hypoxia were small and characteristic of spontaneously transient outward currents. The average resting membrane potential (RMP) was −36 ± 3 mV and could be depolarized by charybdotoxin (100 nM) or tetraethylammonium chloride (5 mM; both blockers of Ca2+-dependent K+ channels) but not by 4-aminopyridine (4-AP; 1 mM; blocker of voltage-gated K+ channels) or glibenclamide (10 μM; blocker of ATP-dependent K+channels). In hypoxia, chelation of intracellular Ca2+ by 5 mM 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid further reduced the amplitude of the whole cell K+ current and prevented spontaneously transient outward current activity. Under these conditions, the remaining current was partially inhibited by 1 mM 4-AP. K+ currents of fetal PASMCs maintained in normoxia were not significantly reduced by acute hypoxia. In normoxic adult PASMCs, whole cell K+ currents were large and RMP was −49 ± 3 mV. These 4-AP-sensitive K+ currents were partially inhibited by exposure to acute hypoxia. We conclude that the K+ channel regulating RMP in the ovine pulmonary circulation changes after birth from a Ca2+-dependent K+ channel to a voltage-dependent K+ channel. The maturational-dependent differences in the mechanism of the response to acute hypoxia may be due to this difference in K+ channels.

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Barbeau, Solène, Guillaume Gilbert, Guillaume Cardouat, Isabelle Baudrimont, Véronique Freund-Michel, Christelle Guibert, Roger Marthan, Pierre Vacher, Jean-François Quignard, and Thomas Ducret. "Mechanosensitivity in Pulmonary Circulation: Pathophysiological Relevance of Stretch-Activated Channels in Pulmonary Hypertension." Biomolecules 11, no. 9 (September 21, 2021): 1389. http://dx.doi.org/10.3390/biom11091389.

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A variety of cell types in pulmonary arteries (endothelial cells, fibroblasts, and smooth muscle cells) are continuously exposed to mechanical stimulations such as shear stress and pulsatile blood pressure, which are altered under conditions of pulmonary hypertension (PH). Most functions of such vascular cells (e.g., contraction, migration, proliferation, production of extracellular matrix proteins, etc.) depend on a key event, i.e., the increase in intracellular calcium concentration ([Ca2+]i) which results from an influx of extracellular Ca2+ and/or a release of intracellular stored Ca2+. Calcium entry from the extracellular space is a major step in the elevation of [Ca2+]i, involving a variety of plasmalemmal Ca2+ channels including the superfamily of stretch-activated channels (SAC). A common characteristic of SAC is that their gating depends on membrane stretch. In general, SAC are non-selective Ca2+-permeable cation channels, including proteins of the TRP (Transient Receptor Potential) and Piezo channel superfamily. As membrane mechano-transducers, SAC convert physical forces into biological signals and hence into a cell response. Consequently, SAC play a major role in pulmonary arterial calcium homeostasis and, thus, appear as potential novel drug targets for a better management of PH.

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Parekh, N., and A. P. Zou. "Role of prostaglandins in renal medullary circulation: response to different vasoconstrictors." American Journal of Physiology-Renal Physiology 271, no. 3 (September 1, 1996): F653—F658. http://dx.doi.org/10.1152/ajprenal.1996.271.3.f653.

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This study investigated effects of renal prostaglandins and their interaction with different vasoactive agents in regulating regional renal blood flow. Using intravenous infusions, we compared effects of different pressor hormones and a nitric oxide (NO) inhibitor under control conditions and after inhibition of cyclooxygenase. Because vasodilator effects of prostanoids are considered to be mediated via opening of ATP-dependent K+ channels, we also studied effects of a prostacyclin analogue (iloprost), a channel opener (lemakalim), and a channel blocker (glibenclamide). Blood flow in renal cortex (CBF) and medulla (MBF) was determined with previously described platinum electrodes inserted into the kidney of anesthetized rats. Angiotensin II and norepinephrine reduced predominantly only CBF (-24 and -19%, respectively). After indomethacin, which selectively reduced MBF (-25%), angiotensin II and norepinephrine also reduced MBF (-45 and -35%, respectively), whereas the corresponding changes in CBF were not affected by indomethacin. Arginine vasopressin and the NO inhibitor NG-nitro-L-arginine methyl ester reduced both CBF and MBF by approximately 30% both under control conditions and after indomethacin. Iloprost and lemakalim increased selectively MBF (15 and 27%, respectively), whereas glibenclamide selectively decreased MBF (-19%). Our data indicate that renal prostaglandins are predominantly involved in regulating medullary circulation. They probably exert their dilatory action on medullary vessels via opening of ATP-dependent K+ channels and are involved in antagonizing medullary effects of pressor hormones in an agonist-specific manner.

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Leffler, Charles W., Helena Parfenova, Jonathan H. Jaggar, and Rui Wang. "Carbon monoxide and hydrogen sulfide: gaseous messengers in cerebrovascular circulation." Journal of Applied Physiology 100, no. 3 (March 2006): 1065–76. http://dx.doi.org/10.1152/japplphysiol.00793.2005.

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This review focuses on two gaseous cellular messenger molecules, CO and H2S, that are involved in cerebrovascular flow regulation. CO is a dilatory mediator in active hyperemia, autoregulation, hypoxic dilation, and counteracting vasoconstriction. It is produced from heme by a constitutively expressed enzyme [heme oxygenase (HO)-2] expressed highly in the brain and by an inducible enzyme (HO-1). CO production is regulated by controlling substrate availability, HO-2 catalytic activity, and HO-1 expression. CO dilates arterioles by binding to heme that is bound to large-conductance Ca2+-activated K+ channels. This binding elevates channel Ca2+ sensitivity, that increases coupling of Ca2+ sparks to large-conductance Ca2+-activated K+ channel openings and, thereby, hyperpolarizes the vascular smooth muscle. In addition to dilating blood vessels, CO can either inhibit or accentuate vascular cell proliferation and apoptosis, depending on conditions. H2S may also function as a cerebrovascular dilator. It is produced in vascular smooth muscle cells by hydrolysis of l-cysteine catalyzed by cystathione γ-lyase (CSE). H2S dilates arterioles at physiologically relevant concentrations via activation of ATP-sensitive K+ channels. In addition to dilating blood vessels, H2S promotes apoptosis of vascular smooth muscle cells and inhibits proliferation-associated vascular remodeling. Thus both CO and H2S modulate the function and the structure of circulatory system. Both the HO-CO and CSE-H2S systems have potential to interact with NO and prostanoids in the cerebral circulation. Much of the physiology and biochemistry of HO-CO and CSE-H2S in the cerebral circulation remains open for exploration.

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Sedivy, Vojtech, Shreena Joshi, Youssef Ghaly, Roman Mizera, Marie Zaloudikova, Sean Brennan, Jana Novotna, Jan Herget, and Alison M. Gurney. "Role of Kv7 channels in responses of the pulmonary circulation to hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 1 (January 1, 2015): L48—L57. http://dx.doi.org/10.1152/ajplung.00362.2013.

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Hypoxic pulmonary vasoconstriction (HPV) is a beneficial mechanism that diverts blood from hypoxic alveoli to better ventilated areas of the lung, but breathing hypoxic air causes the pulmonary circulation to become hypertensive. Responses to airway hypoxia are associated with depolarization of smooth muscle cells in the pulmonary arteries and reduced activity of K+channels. As Kv7 channels have been proposed to play a key role in regulating the smooth muscle membrane potential, we investigated their involvement in the development of HPV and hypoxia-induced pulmonary hypertension. Vascular effects of the selective Kv7 blocker, linopirdine, and Kv7 activator, flupirtine, were investigated in isolated, saline-perfused lungs from rats maintained for 3–5 days in an isobaric hypoxic chamber (FiO2= 0.1) or room air. Linopirdine increased vascular resistance in lungs from normoxic, but not hypoxic rats. This effect was associated with reduced mRNA expression of the Kv7.4 channel α-subunit in hypoxic arteries, whereas Kv7.1 and Kv7.5 were unaffected. Flupirtine had no effect in normoxic lungs but reduced vascular resistance in hypoxic lungs. Moreover, oral dosing with flupirtine (30 mg/kg/day) prevented short-term in vivo hypoxia from increasing pulmonary vascular resistance and sensitizing the arteries to acute hypoxia. These findings suggest a protective role for Kv7.4 channels in the pulmonary circulation, limiting its reactivity to pressor agents and preventing hypoxia-induced pulmonary hypertension. They also provide further support for the therapeutic potential of Kv7 activators in pulmonary vascular disease.

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Pires, Paulo W., Carla M. Dams Ramos, Nusrat Matin, and Anne M. Dorrance. "The effects of hypertension on the cerebral circulation." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 12 (June 15, 2013): H1598—H1614. http://dx.doi.org/10.1152/ajpheart.00490.2012.

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Maintenance of brain function depends on a constant blood supply. Deficits in cerebral blood flow are linked to cognitive decline, and they have detrimental effects on the outcome of ischemia. Hypertension causes alterations in cerebral artery structure and function that can impair blood flow, particularly during an ischemic insult or during periods of low arterial pressure. This review will focus on the historical discoveries, novel developments, and knowledge gaps in 1) hypertensive cerebral artery remodeling, 2) vascular function with emphasis on myogenic reactivity and endothelium-dependent dilation, and 3) blood-brain barrier function. Hypertensive artery remodeling results in reduction in the lumen diameter and an increase in the wall-to-lumen ratio in most cerebral arteries; this is linked to reduced blood flow postischemia and increased ischemic damage. Many factors that are increased in hypertension stimulate remodeling; these include the renin-angiotensin-aldosterone system and reactive oxygen species levels. Endothelial function, vital for endothelium-mediated dilation and regulation of myogenic reactivity, is impaired in hypertension. This is a consequence of alterations in vasodilator mechanisms involving nitric oxide, epoxyeicosatrienoic acids, and ion channels, including calcium-activated potassium channels and transient receptor potential vanilloid channel 4. Hypertension causes blood-brain barrier breakdown by mechanisms involving inflammation, oxidative stress, and vasoactive circulating molecules. This exposes neurons to cytotoxic molecules, leading to neuronal loss, cognitive decline, and impaired recovery from ischemia. As the population ages and the incidence of hypertension, stroke, and dementia increases, it is imperative that we gain a better understanding of the control of cerebral artery function in health and disease.

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Hebert, Steven C., Gary Desir, Gerhard Giebisch, and Wenhui Wang. "Molecular Diversity and Regulation of Renal Potassium Channels." Physiological Reviews 85, no. 1 (January 2005): 319–71. http://dx.doi.org/10.1152/physrev.00051.2003.

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K+ channels are widely distributed in both plant and animal cells where they serve many distinct functions. K+ channels set the membrane potential, generate electrical signals in excitable cells, and regulate cell volume and cell movement. In renal tubule epithelial cells, K+ channels are not only involved in basic functions such as the generation of the cell-negative potential and the control of cell volume, but also play a uniquely important role in K+ secretion. Moreover, K+ channels participate in the regulation of vascular tone in the glomerular circulation, and they are involved in the mechanisms mediating tubuloglomerular feedback. Significant progress has been made in defining the properties of renal K+ channels, including their location within tubule cells, their biophysical properties, regulation, and molecular structure. Such progress has been made possible by the application of single-channel analysis and the successful cloning of K+ channels of renal origin.

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Walker, B. R. "Evidence for uneven distribution of L-type calcium channels in rat pulmonary circulation." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 6 (December 1, 1995): H2051—H2056. http://dx.doi.org/10.1152/ajpheart.1995.269.6.h2051.

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Experiments were performed on isolated, perfused rat lungs to determine the segmental sites of vasoconstriction in response to factors that open voltage-sensitive, L-type calcium channels on vascular smooth muscle cells. Lungs from male Sprague-Dawley rats were perfused at constant flow with a physiological saline solution (PSS) containing albumin. Measurements were made of pulmonary arterial and venous pressure, whereas capillary pressure was estimated by the double-occlusion technique. After equilibration, lungs were constricted with depolarizing PSS containing high K+ (35 or 45 mM). With both stimuli, approximately 80% of the observed increase in vascular resistance occurred on the arterial side of the circulation. Both nifedipine and verapamil reversed this response; however, reversal was more consistent in the arterial segment. In additional experiments, the L-type channel activator (-)BAY K 8644 caused increased resistance in the arterial but not the venous segment. Another group of lungs constricted with the thromboxane mimetic U-46619 demonstrated equal arterial and venous vasoconstriction. In U-46619-constricted lungs, nifedipine caused a 28% reversal of the agonist-induced increase in arterial resistance but was without effect on the venous circulation. These data suggest that a greater density of L-type calcium channels may exist within the arterial segment of the pulmonary circulation than in the veins.

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Olschewski, Andrea, and Edward Kenneth Weir. "Redox Regulation of Ion Channels in the Pulmonary Circulation." Antioxidants & Redox Signaling 22, no. 6 (February 20, 2015): 465–85. http://dx.doi.org/10.1089/ars.2014.5899.

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Termini, D., and T. Moramarco. "Application of entropic approach to estimate the mean flow velocity and Manning roughness coefficient in a high-curvature flume." Hydrology Research 48, no. 3 (December 5, 2016): 634–45. http://dx.doi.org/10.2166/nh.2016.106.

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The entropy-based approach allows the estimation of the mean flow velocity in open channel flow by using the maximum flow velocity. The linear relationship between the mean velocity, umax, and the mean flow velocity, um, through the dimensionless parameter Φ(M), has been verified both in natural rivers and in laboratory channels. Recently, the authors of this study investigated the reliability of the entropy-based formula in a straight channel and under different bed and side-walls' roughness conditions. The present study aims to further validate the entropy-based approach and to explore the effectiveness of entropy-based formula in high curvature channels. Results show that as the effect of the downstream variation of the channel's curvature the value of the parameter Φ(M) varies along the bend. When the bed deformation is evident, the variation of the parameter Φ(M) is strongly reduced compared to that obtained in absence of bed deformation. Results also show that the Manning's roughness coefficients determined through entropy-based formula are in agreement with those estimated by applying other literature's expressions but, unlike the latter, through the parameter Φ(M) the entropy-based formula could account for the effects due to the advective momentum transport by cross-circulation along the strongly curved reaches of the channel.

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Zhang, Qian, Chunyan Li, Wei Huang, Jun Lin, Matthew Hiatt, and Victor H. Rivera-Monroy. "Water Circulation Driven by Cold Fronts in the Wax Lake Delta (Louisiana, USA)." Journal of Marine Science and Engineering 10, no. 3 (March 13, 2022): 415. http://dx.doi.org/10.3390/jmse10030415.

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Atmospheric cold fronts can periodically generate storm surges and affect sediment transport in the Northern Gulf of Mexico (NGOM). In this paper, we evaluate water circulation spatiotemporal patterns induced by six atmospheric cold front events in the Wax Lake Delta (WLD) in coastal Louisiana using the 3-D hydrodynamic model ECOM-si. Model simulations show that channelized and inter-distributary water flow is significantly impacted by cold fronts. Water volume transport throughout the deltaic channel network is not just constrained to the main channels but also occurs laterally across channels accounting for about a quarter of the total flow. Results show that a significant landward flow occurs across the delta prior to the frontal passage, resulting in a positive storm surge on the coast. The along-channel current velocity dominates while cross-channel water transport occurs at the southwest lobe during the post-frontal stage. Depending on local weather conditions, the cold-front-induced flushing event lasts for 1.7 to 7 days and can flush 32–76% of the total water mass out of the system, a greater range of variability than previous reports. The magnitude of water flushed out of the system is not necessarily dependent on the duration of the frontal events. An energy partitioning analysis shows that the relative importance of subtidal energy (10–45% of the total) and tidal energy (20–70%) varies substantially from station to station and is linked to the weather impact. It is important to note that within the WLD region, the weather-induced subtidal energy (46–66% of the total) is much greater than the diurnal tidal energy (13–25% of the total). The wind associated with cold fronts in winter is the main factor controlling water circulation in the WLD and is a major driver in the spatial configuration of the channel network and delta progradation rates.

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Bratz, Ian N., Gregory M. Dick, Johnathan D. Tune, Jason M. Edwards, Zachary P. Neeb, U. Deniz Dincer, and Michael Sturek. "Impaired capsaicin-induced relaxation of coronary arteries in a porcine model of the metabolic syndrome." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 6 (June 2008): H2489—H2496. http://dx.doi.org/10.1152/ajpheart.01191.2007.

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Recent studies implicate channels of the transient receptor potential vanilloid family (e.g., TRPV1) in regulating vascular tone; however, little is known about these channels in the coronary circulation. Furthermore, it is unclear whether metabolic syndrome alters the function and/or expression of TRPV1. We tested the hypothesis that TRPV1 mediates coronary vasodilation through endothelium-dependent mechanisms that are impaired by the metabolic syndrome. Studies were conducted on coronary arteries from lean and obese male Ossabaw miniature swine. In lean pigs, capsaicin, a TRPV1 agonist, relaxed arteries in a dose-dependent manner (EC50 = 116 ± 41 nM). Capsaicin-induced relaxation was blocked by the TRPV1 antagonist capsazepine, endothelial denudation, inhibition of nitric oxide synthase, and K+ channel antagonists. Capsaicin-induced relaxation was impaired in rings from pigs with metabolic syndrome (91 ± 4% vs. 51 ± 10% relaxation at 100 μM). TRPV1 immunoreactivity was prominent in coronary endothelial cells. TRPV1 protein expression was decreased 40 ± 11% in obese pigs. Capsaicin (100 μM) elicited divalent cation influx that was abolished in endothelial cells from obese pigs. These data indicate that TRPV1 channels are functionally expressed in the coronary circulation and mediate endothelium-dependent vasodilation through a mechanism involving nitric oxide and K+ channels. Impaired capsaicin-induced vasodilation in the metabolic syndrome is associated with decreased expression of TRPV1 and cation influx.

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Burchard, Hans, Robert D. Hetland, Elisabeth Schulz, and Henk M. Schuttelaars. "Drivers of Residual Estuarine Circulation in Tidally Energetic Estuaries: Straight and Irrotational Channels with Parabolic Cross Section." Journal of Physical Oceanography 41, no. 3 (March 1, 2011): 548–70. http://dx.doi.org/10.1175/2010jpo4453.1.

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Abstract The generation of residual circulation in a tidally energetic estuary with constant longitudinal salinity gradient and parabolic cross section is examined by means of a two-dimensional cross-sectional numerical model, neglecting river runoff and Stokes drift. It is shown how the longitudinal and lateral residual circulation can be decomposed into contributions from various processes such as tidal straining circulation, gravitational circulation, advectively driven circulation, and horizontal mixing circulation. The sensitivity of the residual circulation and its components from various processes to changes in forcing is investigated by varying the Simpson number (nondimensional longitudinal buoyancy gradient) and the unsteadiness parameter (nondimensional tidal frequency), as well as the bed roughness and the width of the estuary. For relatively weak salinity gradient forcing, the tidal straining circulation dominates the residual exchange circulation in support of classical estuarine circulation (up-estuary flow near the bed and down-estuary flow near the surface). The strength of the longitudinal estuarine circulation clearly increases with increased salinity gradient forcing. However, when the Simpson number exceeds 0.15, the relative contributions of both gravitational circulation and advectively driven circulation to estuarine circulation increase substantially. Lateral residual circulation is relatively weak for small Simpson numbers and becomes flood oriented (divergent flow near the bed and convergent flow near the surface) for larger Simpson numbers because of increasing contributions from gravitational and advectively driven circulation. Increasing the unsteadiness number leads to decreased longitudinal and lateral residual circulation. Although changes in bed roughness result in relatively small changes in residual circulation, results are sensitive to the width of the estuary, mainly because of changes in residual exchange circulation driven by tidal straining.

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Cornfield, D. N., J. A. McQueston, I. F. McMurtry, D. M. Rodman, and S. H. Abman. "Role of ATP-sensitive potassium channels in ovine fetal pulmonary vascular tone." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 5 (November 1, 1992): H1363—H1368. http://dx.doi.org/10.1152/ajpheart.1992.263.5.h1363.

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To study the potential role of ATP-sensitive K+ (K+ATP) channels in fetal pulmonary vasoregulation, we studied the effect of a K+ATP channel agonist, lemakalim, and antagonist, glibenclamide, on the fetal pulmonary circulation in nine chronically instrumented late-gestation fetal lambs. Left pulmonary artery (LPA) blood flow was measured with an electromagnetic flow transducer. Brief (10 min) infusions of lemakalim at 3, 10, and 30 micrograms/min into the LPA produced dose-dependent increases in flow from 68 +/- 7 to 96 +/- 11, 160 +/- 15, and 204 +/- 34 ml/min, respectively. The duration of pulmonary vasodilation after the 10-min infusions of lemakalim at 3, 10, and 30 micrograms/min was 20 +/- 3, 47 +/- 10, and 55 +/- 15 min, respectively. Pulmonary blood pressure and flow did not change with intrapulmonary infusion of glibenclamide (10 mg), a K+ATP channel antagonist. Lemakalim-induced pulmonary vasodilation was not affected by nitro-L-arginine (10 mg), a competitive inhibitor of endothelium-dependent relaxing factor, but was blocked by glibenclamide. Prolonged (2 h) intrapulmonary infusions of lemakalim (2-6 micrograms/min) increased pulmonary blood flow by 137%. The increase in pulmonary blood flow was sustained throughout the infusion. Systemic and pulmonary arterial pressures decreased during prolonged infusion. We conclude that K+ATP channels are present in the fetal pulmonary circulation, but do not participate in the regulation of basal pulmonary vascular tone. K+ATP channel activation produces sustained vasodilation that is not mediated by endothelium-derived relaxing factor. We speculate that birth-related stimuli activate K+ATP channels to enhance the pulmonary vasodilation that occurs at birth.

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33

Dick, Gregory M., Ian N. Bratz, Léna Borbouse, Gregory A. Payne, Ü. Deniz Dincer, Jarrod D. Knudson, Paul A. Rogers, and Johnathan D. Tune. "Voltage-dependent K+ channels regulate the duration of reactive hyperemia in the canine coronary circulation." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (May 2008): H2371—H2381. http://dx.doi.org/10.1152/ajpheart.01279.2007.

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We previously demonstrated a role for voltage-dependent K+ (KV) channels in coronary vasodilation elicited by myocardial metabolism and exogenous H2O2, as responses were attenuated by the KV channel blocker 4-aminopyridine (4-AP). Here we tested the hypothesis that KV channels participate in coronary reactive hyperemia and examined the role of KV channels in responses to nitric oxide (NO) and adenosine, two putative mediators. Reactive hyperemia (30-s occlusion) was measured in open-chest dogs before and during 4-AP treatment [intracoronary (ic), plasma concentration 0.3 mM]. 4-AP reduced baseline flow 34 ± 5% and inhibited hyperemic volume 32 ± 5%. Administration of 8-phenyltheophylline (8-PT; 0.3 mM ic or 5 mg/kg iv) or NG-nitro-l-arginine methyl ester (l-NAME; 1 mg/min ic) inhibited early and late portions of hyperemic flow, supporting roles for adenosine and NO. 4-AP further inhibited hyperemia in the presence of 8-PT or l-NAME. Adenosine-induced blood flow responses were attenuated by 4-AP (52 ± 6% block at 9 μg/min). Dilation of arterioles to adenosine was attenuated by 0.3 mM 4-AP and 1 μM correolide, a selective KV1 antagonist (76 ± 7% and 47 ± 2% block, respectively, at 1 μM). Dilation in response to sodium nitroprusside, an NO donor, was attenuated by 4-AP in vivo (41 ± 6% block at 10 μg/min) and by correolide in vitro (29 ± 4% block at 1 μM). KV current in smooth muscle cells was inhibited by 4-AP (IC50 1.1 ± 0.1 mM) and virtually eliminated by correolide. Expression of mRNA for KV1 family members was detected in coronary arteries. Our data indicate that KV channels play an important role in regulating resting coronary blood flow, determining duration of reactive hyperemia, and mediating adenosine- and NO-induced vasodilation.

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34

Mishra, Ashish Mani, and Suneet Singh. "Non linear stability analysis of parallel channels with natural circulation." Nuclear Engineering and Design 309 (December 2016): 136–50. http://dx.doi.org/10.1016/j.nucengdes.2016.09.002.

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35

Zhou, T., S. Qi, M. Song, and Z. Xiao. "Experimental study of natural circulation flow instability in rectangular channels." Kerntechnik 82, no. 2 (April 27, 2017): 184–89. http://dx.doi.org/10.3139/124.110654.

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36

TAKEDA, Tetsuaki, Hiroshi KAWAMURA, and Masahiro SEKI. "Natural circulation in parallel vertical channels with different heat inputs." Transactions of the Japan Society of Mechanical Engineers Series B 52, no. 480 (1986): 3035–42. http://dx.doi.org/10.1299/kikaib.52.3035.

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37

Stashchuk, Nataliya, Vasiliy Vlasenko, and Toby J. Sherwin. "Numerical investigation of deep water circulation in the Faroese Channels." Deep Sea Research Part I: Oceanographic Research Papers 58, no. 7 (July 2011): 787–99. http://dx.doi.org/10.1016/j.dsr.2011.05.005.

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38

Takeda, T., H. Kawamura, and M. Seki. "Natural circulation in parallel vertical channels with different heat inputs." Nuclear Engineering and Design 104, no. 2 (October 1987): 133–43. http://dx.doi.org/10.1016/0029-5493(87)90294-9.

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39

Egashira, Kensuke, Yousuke Katsuda, and Akira Takeshita. "ATP-sensitive K+ channels and metabolic vasodilation in coronary circulation." Pathophysiology 1 (November 1994): 303. http://dx.doi.org/10.1016/0928-4680(94)90623-8.

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40

Kao, Yang-Ta, Hsiau-Wen Lin, and Dai-Yi Qiu. "Implementation of Offline Consumer Behavior Tracking." International Journal of Pattern Recognition and Artificial Intelligence 35, no. 09 (May 4, 2021): 2150028. http://dx.doi.org/10.1142/s0218001421500282.

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Due to declining trading volume growth in e-commerce platforms, physical channels have attracted considerable investments from various large international companies (e.g. Alibaba, JD, Walmart, Wanda, and Wuzhou International). However, e-commerce platforms can track consumers’ behaviors (attraction to landing page design, clicks on certain products, consumer behavior trajectory tracking, clicks on advertisements, and internal link optimization of product pages), a feat unachievable in current physical channels. Consequently, this study attempted to apply the characteristics of online channels in a physical channel by using image object tracking and image detection techniques. Through this inclusion, physical channels are capable of providing consumers with more favorable experience and interaction, and brick-and-mortar store owners can obtain a more accurate understanding of consumer behaviors of store consumers. Information acquired through this system can be provided to store owners to serve as reference for merchandise placement, arrangement of display shelves, and consumer circulation path planning. This study used the technique of image processing to locate the Region of Interest and applied object tracking to get the consumer’s trajectory which successfully implemented the consumer-tracking characteristics of online platforms in a physical channel while retaining the unique experience of the physical channel. This results in a win–win scenario for businesses and consumers.

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41

Jeffries, Martin O., and M. Amanda Shaw. "The drift of ice islands from the Arctic Ocean into the channels of the Canadian Arctic archipelago: the history of Hobson's Choice Ice Island." Polar Record 29, no. 171 (October 1993): 305–12. http://dx.doi.org/10.1017/s0032247400023950.

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ABSTRACTThe drift of Hobson's Choice Ice Island from the Arctic Ocean into the channels of the Queen Elizabeth Islands, Northwest Territories, Canadian Arctic, between February 1988 and August 1992, was monitored by a Système Argos satellite-positioning buoy. During the period August 1991 to May 1992, the ice island was imaged by synthetic aperture radar (SAR) aboard the ERS-1 satellite. The buoy data show that Hobson's Choice entered Peary Channel (between Axel Heiberg Island and Ellef Ringnes Island) in October 1988. Subsequently, between mid-August 1991 and November 1991, it drifted rapidly south to Queens Channel (60 km north of Cornwallis Island). The SAR data corroborate the buoy data and also reveal that at least six other ice islands entered the Queen Elizabeth Islands' channels with Hobson's Choice. The SAR imagery also recorded the fragmentation of Hobson's Choice between mid-October and mid-November 1991. The buoy and SAR data are conclusive evidence that ice islands do leave the Arctic Ocean via the northwestern channels of the Canadian Arctic archipelago. The observed drift occurred when there was extensive break-up of fast ice in the inter-island channels caused by above average summer temperatures, in combination with favourable atmospheric circulation and surface winds that drove the ice islands into and through the channels.

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42

Jouen-Tachoire, Thibault R. H., Stephen J. Tucker, and Paolo Tammaro. "Ion channels as convergence points in the pathology of pulmonary arterial hypertension." Biochemical Society Transactions 49, no. 4 (August 4, 2021): 1855–65. http://dx.doi.org/10.1042/bst20210538.

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Pulmonary arterial hypertension (PAH) is a fatal disease of the cardiopulmonary system that lacks curative treatments. The main pathological event in PAH is elevated vascular resistance in the pulmonary circulation, caused by abnormal vasoconstriction and vascular remodelling. Ion channels are key determinants of vascular smooth muscle tone and homeostasis, and four PAH channelopathies (KCNK3, ABCC8, KCNA5, TRPC6) have been identified so far. However, the contribution of ion channels in other forms of PAH, which account for the majority of PAH patients, has been less well characterised. Here we reason that a variety of triggers of PAH (e.g. BMPR2 mutations, hypoxia, anorectic drugs) that impact channel function may contribute to the onset of the disease. We review the molecular mechanisms by which these ‘extrinsic’ factors converge on ion channels and provoke their dysregulation to promote the development of PAH. Ion channels of the pulmonary vasculature are therefore promising therapeutic targets because of the modulation they provide to both vasomotor tone and proliferation of arterial smooth muscle cells.

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Butler, J. P., J. Huang, S. H. Loring, S. J. Lai-Fook, P. M. Wang, and T. A. Wilson. "Model for a pump that drives circulation of pleural fluid." Journal of Applied Physiology 78, no. 1 (January 1, 1995): 23–29. http://dx.doi.org/10.1152/jappl.1995.78.1.23.

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Physical and mathematical models were used to study a mechanism that could maintain the layer of pleural fluid that covers the surface of the lung. The pleural space was modeled as a thin layer of viscous fluid lying between a membrane carrying tension (T), representing the lung, and a rigid wall, representing the chest wall. Flow of the fluid was driven by sliding between the membrane and wall. The physical model consisted of a cylindrical balloon with strings stretched along its surface. When the balloon was inflated inside a vertical circular cylinder containing a viscous fluid, the strings formed narrow vertical channels between broad regions in which the balloon pressed against the outer cylinder. The channels simulated the pleural space in the regions of lobar margins. Oscillatory rotation of the outer cylinder maintained a lubricating layer of fluid between the balloon and the cylinder. The thickness of the fluid layer (h), measured by fluorescence videomicroscopy, was larger for larger fluid viscosity (mu), larger sliding velocity (U), and smaller pressure difference (delta P) between the layer and the channel. A mathematical model of the flow in a horizontal section was analyzed, and numerical solutions were obtained for parameter values of mu, U, delta P, and T that matched those of the physical model. The computed results agreed reasonably well with the experimental results. Scaling laws yield the prediction that h is approximately (T/delta P)(microU/T)2/3. For physiological values of the parameters, the predicted value of h is approximately 10(-3) cm, in good agreement with the observed thickness of the pleural space.

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Perreault, T., and J. De Marte. "Maturational changes in endothelium-derived relaxations in newborn piglet pulmonary circulation." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 2 (February 1, 1993): H302—H309. http://dx.doi.org/10.1152/ajpheart.1993.264.2.h302.

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It is accepted knowledge that the endothelium can profoundly affect vascular tone through the release of vasoactive substances. The maturational changes in the role of the endothelium-derived relaxing factor (EDRF) and ATP-dependent K+ channels in the neonatal pulmonary circulation were investigated in isolated perfused lungs from 1- and 7-day-old piglets. The EDRF inhibitor, N omega-nitro-L-arginine (L-NNA), had potent dose-dependent constrictor effects on the pulmonary vasculature with normal and raised tone. The constrictor effect of L-NNA was greater (P < 0.05) in the 1-day-old than in the 7-day-old lungs and was significantly (P < 0.005) attenuated by pretreatment with the EDRF precursor, L-arginine. Furthermore, we studied the possibility of developmental changes in the sensitivity of smooth muscle cells to EDRF by testing sodium nitroprusside, nitric oxide, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP). All caused a decrease in perfusion pressure, but only sodium nitroprusside elicited a greater (P < 0.01) effect in the 1-day-old. Endothelin-1 (ET-1) and bradykinin (BK) elicited dilator responses that were significantly (P < 0.05) reduced in the presence of L-NNA. Interestingly, the dilator response to ET-1 was more marked (P < 0.001) in the younger group, whereas no age difference was noted with BK. Finally, lemakalim, a K+ channel activator, caused a vasodilation of equal magnitude at both ages. In summary, EDRF and ATP-dependent K+ channels appear to play a role in the control of the newborn piglet pulmonary vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

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McDaniel, Sharon S., Oleksandr Platoshyn, Ying Yu, Michele Sweeney, Victor A. Miriel, Vera A. Golovina, Stefanie Krick, Bethany R. Lapp, Jian-Ying Wang, and Jason X. J. Yuan. "Anorexic effect of K+ channel blockade in mesenteric arterial smooth muscle and intestinal epithelial cells." Journal of Applied Physiology 91, no. 5 (November 1, 2001): 2322–33. http://dx.doi.org/10.1152/jappl.2001.91.5.2322.

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Activity of voltage-gated K+ (Kv) channels controls membrane potential ( E m). Membrane depolarization due to blockade of K+ channels in mesenteric artery smooth muscle cells (MASMC) should increase cytoplasmic free Ca2+ concentration ([Ca2+]cyt) and cause vasoconstriction, which may subsequently reduce the mesenteric blood flow and inhibit the transportation of absorbed nutrients to the liver and adipose tissue. In this study, we characterized and compared the electrophysiological properties and molecular identities of Kv channels and examined the role of Kv channel function in regulating E m in MASMC and intestinal epithelial cells (IEC). MASMC and IEC functionally expressed multiple Kv channel α- and β-subunits (Kv1.1, Kv1.2, Kv1.3, Kv1.4, Kv1.5, Kv2.1, Kv4.3, and Kv9.3, as well as Kvβ1.1, Kvβ2.1, and Kvβ3), but only MASMC expressed voltage-dependent Ca2+ channels. The current density and the activation and inactivation kinetics of whole cell Kv currents were similar in MASMC and IEC. Extracellular application of 4-aminopyridine (4-AP), a Kv-channel blocker, reduced whole cell Kv currents and caused E m depolarization in both MASMC and IEC. The 4-AP-induced E m depolarization increased [Ca2+]cyt in MASMC and caused mesenteric vasoconstriction. Furthermore, ingestion of 4-AP significantly reduced the weight gain in rats. These results suggest that MASMC and IEC express multiple Kv channel α- and β-subunits. The function of these Kv channels plays an important role in controlling E m. The membrane depolarization-mediated increase in [Ca2+]cyt in MASMC and mesenteric vasoconstriction may inhibit transportation of absorbed nutrients via mesenteric circulation and limit weight gain.

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Gan, Wei, and Bo Huang. "Exploring Data Integrity of Dual-Channel Supply Chain Using Blockchain Technology." Computational Intelligence and Neuroscience 2022 (May 18, 2022): 1–13. http://dx.doi.org/10.1155/2022/3838282.

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The study intends to solve the problems of complex product circulation caused by information asymmetry and the untimely communication of production and sales information in the process of product sales to reduce the cost in the process of product circulation. Based on blockchain technology, the data integrity of the dual-channel supply chain is studied. First, the data of the supply chain conduct coordinated management to achieve the integrity of the supply chain data. Then, under the background that both retailers and suppliers are risk-neutral individuals, the benchmark model of the dual-channel supply chain is constructed, and the online and offline sales prices of products under different decision-making modes are analyzed. Finally, taking fresh agricultural products as an example, the sales strategies of the online and offline sales channels of fresh agricultural products are studied, and a dual-channel supply chain model is constructed. The profit of each member in the supply chain system under this model is obtained by the inverse method. The simulation results demonstrate that the retailer’s revenue and the total revenue of the system increase obviously with the growth of the price discount coefficient after the price discount strategy is applied. When the compensation cost is between 1,000 and 3,000, the profit of retailers in the supply chain system is improved by using the price coordination mechanism, while the profit of suppliers decreases to some extent. When the value of compensation cost is 7,000–9,000, the application of the price coordination mechanism increases the profit of suppliers in the supply chain system, while the profit of retailers declines to a certain extent. The research content reported here effectively alleviates the profit conflict and the double marginal effect between the two channels and enriches the theoretical system knowledge of the coordination of the two channels’ supply chain of agricultural products.

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Yung, Kaung-Ti. "A Birdcage Model for the Chinese Meridian System Part VI: Meridians as the Primary Regulatory System." American Journal of Chinese Medicine 33, no. 05 (January 2005): 759–66. http://dx.doi.org/10.1142/s0192415x05003302.

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It is imperative to define the fundamental concepts of Qi, channels, and the meridian system of Chinese medicine in terms of scientific terminology before any meaningful and mutually beneficial dialog can begin between Chinese and Western medicine. In the Chinese theory, the meridian system as a whole is the system of the body. We propose the existence of a meridian regulatory system that governs interactions between and adjusts functions of internal organs, connects them to the body surface through a network of pathways (channels) and displays their status on the skin. The meridian systems is analyzed as a 28-leg, uniform, low pass birdcage coil, where each leg represents a channel. The channel is analyzed as a transmission line and Qi is the standing wave riding on it. Each segment in the channel is represented as a section of the transmission line and it is in natural oscillation, with its second lowest resonant frequency being the 50-round circulation frequency f50, 0.578 × 10-3 Hz .

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Bahaidarah, Haitham, and Ahmet Sahin. "Thermodynamic analysis of fluid flow in channels with wavy sinusoidal walls." Thermal Science 17, no. 3 (2013): 813–22. http://dx.doi.org/10.2298/tsci110403200b.

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Entropy generation in channels with non-uniform cross-section that can be found in many fluid flow systems is an important concern from the thermodynamic design point of view. In this regard, the entropy generation in channels with periodic wavy sinusoidal walls has been considered in present study. The flow is assumed to be two-dimensional steady laminar and the main parameters considered are the Re number, height ratio Hmin/Hmax and module length ratio L/a. The fluid enters the channel with uniform axial velocity and temperature. The wall of the channel is assumed to be at uniform temperature which is different that of the fluid at the inlet of the channel. The distribution of the entropy generation as well as the total entropy generation has been studied numerically. It is found that the Re number and the geometric parameters, height ratio and module length ratio have significant effect on both the local concentrations of entropy generation as well as the total entropy generation in the channel. Flow separation and re-circulation size, strength and location of flow are found to be major concern in determining the local entropy generation.

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Patel, Shalinkumar, Alexander L. Fedinec, Jiangxiong Liu, Max A. Weiss, Massroor Pourcyrous, Mimily Harsono, Helena Parfenova, and Charles W. Leffler. "H2S mediates the vasodilator effect of endothelin-1 in the cerebral circulation." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (December 1, 2018): H1759—H1764. http://dx.doi.org/10.1152/ajpheart.00451.2018.

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H2S is an endogenous gasotransmitter that increases cerebral blood flow. In the cerebral vascular endothelium, H2S is produced by cystathionine δ-lyase (CSE). Endothelin-1 (ET-1) has constrictor and dilator influences on the cerebral circulation. The mechanism of the vasodilation caused by ET-1 may involve endothelium-derived factors. We hypothesize that ET-1-elicited dilation of pial arterioles requires an elevation of H2S production in the cerebral vascular endothelium. We investigated the effects of ET-1 on CSE-catalyzed brain H2S production and pial arteriolar diameter using cranial windows in newborn pigs in vivo. H2S was measured in periarachnoid cerebrospinal fluid. ET-1 (10−12–10−8 M) caused an elevation of H2S that was reduced by the CSE inhibitors propargylglycine (PPG) and β-cyano-l-alanine (BCA). Low doses of ET-1 (10−12–10−11 M) produced vasodilation of pial arterioles that was blocked PPG and BCA, suggesting the importance of H2S influences. The vasodilator effects of H2S may require activation of smooth muscle cell membrane ATP-sensitive K+ (KATP) channels and large-conductance Ca2+-activated K+ (BK) channels. The KATP inhibitor glibenclamide and the BK inhibitor paxilline blocked CSE/H2S-dependent dilation of pial arterioles to ET-1. In contrast, the vasoconstrictor response of pial arterioles to 10−8 M ET-1 was not modulated by PPG, BCA, glibenclamide, or paxilline and, therefore, was independent of CSE/H2S influences. Pial arteriolar constriction response to higher levels of ET-1 was independent of CSE/H2S and KATP/BKCa channel activation. These data suggest that H2S is an endothelium-derived factor that mediates the vasodilator effects of ET-1 in the cerebral circulation via a mechanism that involves activation of KATP and BK channels in vascular smooth muscle. NEW & NOTEWORTHY Disorders of the cerebral circulation in newborn infants may lead to lifelong neurological disabilities. We report that vasoactive peptide endothelin-1 exhibits vasodilator properties in the neonatal cerebral circulation by stimulating production of H2S, an endothelium-derived messenger with vasodilator properties. The ability of endothelin-1 to stimulate brain production of H2S may counteract the reduction in cerebral blood flow and prevent the cerebral vascular dysfunction caused by stroke, asphyxia, cerebral hypoxia, ischemia, and vasospasm.

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Straffin, E. C., and M. D. Blum. "Holocene fluvial response to climate change and human activities; Burgundy, France." Netherlands Journal of Geosciences - Geologie en Mijnbouw 81, no. 3-4 (December 2002): 417–30. http://dx.doi.org/10.1017/s0016774600022691.

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AbstractAlluvial deposits of the Loire/Arroux trunk/tributary system record distinct, synchronous episodes of regional fluvial adjustment. Changes in facies and depositional style through time can be interpreted with a modern analogue model that relates vegetative cover/human influence with sediment supply, and modes of atmospheric circulation with the paths and styles of storms that drive variable discharge regimes across western Europe.Zonal atmospheric circulation results in a Mediterranean style climate over southern Burgundy, producing dry conditions punctuated by infrequent, large floods. Episodic overbank sedimentation and the burial of thin paleosols in sandy overbank facies is indicative of this style of fluvial activity, ca 1300 years BP. Humans may have increased the available volume of fine grained sediment at this times through increased agricultural activity along valley axes, however facies match that expected from a ‘flashy’ discharge regime.In contrast, meridional circulation patterns result in a maritime style climate over southern Burgundy, with the intrusion of storms, moist conditions and frequent, moderate magnitude discharges. Wide, deep channels, thick channel facies and thin overbank facies are indicative of this style of fluvial activity, recorded in deposits dating to ca 4050 to 3200 years BP. Strong meridional conditions and extreme climatic variability during the Little Ice Age resulted in very large discharges that straightened and widened channels, while scouring and obscuring older terraces (ca 500 years BP). Deposition over the last two centuries is related to increasingly zonal circulation and infrequent, large (over-bank) floods. Changes in fluvial dynamics over the last 300 years can be attributed primarily to climatic control, as there has been very little change in land-use over that period.

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Journal articles on the topic 'Circulation channels'

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